Publications by authors named "Kazunori Uegaki"

Background: We performed a retrospective study to clarify the outcome of stage IB2-IIB patients with bulky cervical cancer who underwent neoadjuvant chemotherapy (NAC) followed by radical hysterectomy and adjuvant treatment.

Methods: Sixty-five patients with bulky stage IB2-IIB cervical cancer, treated at Tottori University Hospital between 2001 and 2011, were examined retrospectively. The indication for adjuvant treatment was limited to the following pathological high-risk factors: pelvic lymph node (PLN) involvement, parametrial infiltration (PI), and a compromised surgical margin.

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Objective: This study was aimed to elucidate the roles of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3'-kinase (PI3K)/Akt pathways in regulating cytotoxicity induced by cisplatin (CDDP) in ovarian carcinoma cells.

Methods: We treated 7 ovarian cancer cell lines with CDDP alone or with CDDP and either a PI3K inhibitor (LY294002), a MEK inhibitor (PD98059), or a MEK/ERK activator (phorbol 12-myristate 13-acetate [PMA]) and assessed cell viability, expression of MEK/ERK and PI3K/Akt, cell cycle distribution, and apoptosis. We also investigated the effect of combination treatment on survival in a xenograft model.

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Purpose: The mTOR pathway is thought to be a central regulator of proliferation and survival of cells. Rapamycin and its analogs are undergoing clinical trials in patients with epithelial ovarian cancer. This study aimed to assess the potential to use rapamycin and anticancer agents in combination for first- and second-line chemotherapy to treat ovarian cancer.

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Objective: Preoperative and intraoperative assessments of myometrial invasion (MI) are commonly used for planning surgical procedures such as dissection of the para-aortic node; however, the assessments often differ from the final diagnosis determined by pathological examination. The present study evaluated the accuracy of preoperative and intraoperative assessments of MI.

Methods: A total of 191 patients with endometrial cancer, who underwent hysterectomy from 1995 to 2007 in Tottori University Hospital, were included in this study.

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Resistance of ovarian mucinous adenocarcinoma to standard chemotherapy with paclitaxel and carboplatin is associated with poor prognosis, and an effective treatment is needed. The present study aimed to identify an effective chemotherapy for ovarian mucinous adenocarcinoma. Five human ovarian mucinous adenocarcinoma cell lines (MN-1, OMC-1, RMUG-L, RMUG-S, TU-OM-1) were used in this study.

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PTEN is involved in the regulation of normal cellular functions in addition to its well-known role as a tumor suppressor. In the present study, we have shown that stable transfection of the PTEN gene into PTEN-mutated endometrial carcinoma cells leads to contact inhibition accompanied by a decreased level of phosphorylated-Akt (p-Akt) expression, an increase in p27(Kip1), and a decrease in beta-catenin. PTEN-induced cells with contact inhibition exhibit G0-G1 cell-cycle arrest, and the Ki-67 labeling index is reduced.

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PTEN and the PI3K/Akt pathway are involved in the development and/or progression of endometrial carcinoma. To clarify the impact of the pathway-related molecules on prognosis, we analyzed PTEN, phosphorylated-Akt (p-Akt), and Ki-67 expression by immunohistochemistry in 99 patients with advanced endometrial carcinoma. PTEN-negative or PTEN-mixed staining was found in 66% of tumors.

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The present study was conducted to determine whether and how expression of the c-myc gene is related to the response to chemotherapy in patients with epithelial ovarian cancer. This study includes 101 consecutive patients with stage Ic to IV epithelial ovarian cancer who underwent primary surgery followed by platinum-based chemotherapy. Immunohistochemical studies were performed to detect Ki-67 and ARF proteins.

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Purpose: The aim of this study was to determine the behavior of docetaxel (DTX) in ovarian cancer cells resistant to paclitaxel (PTX).

Methods: We used human ovarian adenocarcinoma cell lines KF, KFTx (PTX-resistant KF), SK-OV-3, and HAC-2. The sensitivity of the cells to PTX or DTX was determined by the MTT assay.

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